Demonstration of a depressor reflex in acute cardiac tamponade

Laboratory studies have demonstrated the presence of a vagally mediated reflex in acute cardiac tamponade. To determine the effect of this reflex on cardiac performance, the authors continuously recorded hemodynamic parameters during induction of tamponade in 16 closed chest mongrel dogs anesthetized with alpha chloralose. The studies were done 1 to 7 days following the insertion of a catheter in the pericardial sac. With increasing pericardial volume, there was a progressive deterioration of cardiac performance, the most marked changes occurring in the late phases of cardiac tamponade. When pericardial, right atrial, and left ventricular end diastolic pressures rose rapidly with the infusion of 198 ± 68 c.c. of fluid, heart rate slowed abruptly and ventricular performance deteriorated precipitously. Administration of atropine at this time produced an improvement in heart rate (p < 0.001), left ventricular systolic pressure (p < 0.001), peak positive dp/dt (p < 0.01), and peak negative dp/dt (p < 0.025). Following administration of atropine, the pericardial sac could accommodate an additional 30 to 90 c.c. of fluid before the appearance of electromechanical dissociation. Also, the increments of left ventricular systolic pressure, peak positive dp/dt, and peak negative dp/dt following atropine were significantly greater than with atrial pacing at a comparable heart rate (210 versus 220, atropine): Δ19 ± 24 versus Δ62 ± 19 mm. Hg, p < 0.02; Δ397 ± 496 versus Δ1,589 ± 452 mm. Hg per second, p < 0.02; and Δ128 ± 314 versus Δ1,228 ± 564 mm. Hg per second, p < 0.25, respectively. This study establishes, therefore, that the activation of a depressor reflex contributes to the deterioration of cardiac performance in the late phase of tamponade.